External validation of the Briganti nomogram to estimate the probability of specimen‐confined disease in patients with high‐risk prostate cancer. (13th August 2014) - Roumiguié, Mathieu
Abstract Objective To establish an external validation of the updated nomogram from Briganti et al., which provides estimates of the probability of specimen‐confined disease using the variables age, prostate‐specific antigen (PSA), clinical stage and biopsy Gleason score in preoperatively defined high‐risk prostate cancer (PCa). Patients and Methods The study included 523 patients with high‐risk PCa, as defined by d'Amico classification, undergoing radical prostatectomy (RP) and bilateral lymph node dissection in one of two academic centres between 1990 and 2013. Specimen‐confined disease was defined as pT2–pT3a node‐negative PCa with negative surgical margins. The receiver–operator characteristic (ROC) curve was obtained to quantify the overall accuracy (area under the curve [AUC]) of the model in predicting specimen‐confined disease. A calibration curve was then constructed to illustrate the relationship between the risk estimates obtained by the model (x‐axis) and the observed proportion of specimen‐confined disease (y‐axis). The Kaplan–Meier method was used to assess biochemical recurrence (BCR)‐free survival. Results Patients' median age and PSA level were 64 years and 21 ng/mL, respectively. The definition of high‐risk PCa was based on PSA level only in 38.3%, a biopsy Gleason score >7 in 34.5%, a clinical stage >T2b in 6.9%, or a combination of these two or three factors in 20.3% of patients. Positive surgical margins were observed in 43.6%, with a rate of 14.8% in pT2 cancers and lymph node metastasis in 12.1% of patients. pT stage was pT0 in 0.9%, pT2 in 28.9%, pT3a in 37.5% and pT3b–4 in 32.7% of patients. Overall, 44.4% of patients (N = 232) had specimen‐confined disease. PSA and cT stage were independently predictive of specimen‐confined disease. The median (range) 2‐, 5‐, and 8‐year BCR‐free survival rates were significantly higher in specimen‐confined disease as compared with non‐specimen‐confined disease: 80.87 (73.67–86.29) vs 37.55 (30.64–44.44)%, 63.53 (52.37–72.74) vs 26.93 (19.97–34.36)% and 55.08 (41.49–66.74) vs 19.52 (12.50–27.70)%, respectively (P < 0.001). The ROC curve analysis showed relevant accuracy of the model (AUC 0.6470, 95% CI 0.60–0.69) although the calibration plot suggested that, for risks ranging from 0.3 to 0.5, the odds of extracapsular extension were underestimated. Conclusions This external validation of the Briganti nomogram shows relevant accuracy, although the relative imprecision for intermediate risk may limit its clinical relevance. Our follow‐up findings confirm the large proportion of specimen‐confined PCa with good oncological outcomes in this heterogeneous subgroup of patients with high‐risk PCa.